Parkinson?s disease (PD) is a debilitating movement disorder that affects over 60,000 new cases per year in the US alone and is characterized by a progressive degeneration of dopamine-releasing neurons that innervate the entire basal ganglia. It is thought that the hypokinetic symptoms of PD arise from an imbalance of the striatal direct pathway and indirect pathways. Our previous work has shown that: 1) the external segment of the globus pallidus (GPe) extensively innervates the dorsal striatum (dStr) and targets both the direct and indirect pathway spiny projection neurons (dSPNs and iSPNs), 2) this GPe-dStr projection arise from the Npas1+ GPe neurons, and 3) the Npas1+ GPe-dStr projection to iSPNs is strengthened preferentially in the chronic 6-hydroxydopamine (6-OHDA) lesion mice?a model of PD. However, the t mechanisms underlying the signaling of the Npas1+ pallidostriatal input to SPNs is not known. Accordingly, how its alterations associated with chronic 6-OHDA lesion is not understood. Most importantly, the function of the Npas1+ GPe-dStr input to SPN is completely unexplored. ?Our overarching hypothesis is that the Npas1+ GPe-dStr projection reduces dendritic excitability of SPNs and this effect becomes strengthened after chronic dopamine depletion by an increase in number of synaptic contacts of Npas1+ GPe-SPN input?. To test these ideas the proposed research will be accomplished using an array of tools, including transgenic mice, optogenetics, ?ex vivo patch-clamp electrophysiology, ?ex vivo calcium imaging, quantitative polymerase chain reaction, and immunohistochemistry.